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McGreevy, P. D., Cripps, P. J., French, N. P., Green, L. E., & Nicol, C. J. (1995). Management factors associated with stereotypic and redirected behaviour in the thoroughbred horse. Equine Vet J, 27(2), 86–91.
Abstract: A greater knowledge of the effect of management factors is required to investigate the ontogeny of abnormal behaviour in the stabled horse. A postal survey of racehorse (flat) trainers yielded information about 22 yard and management factors. The relationship of the factors to the prevalence of abnormal behaviour was analysed by logistic regression. Management factors related to the time spent in the stable showed the strongest associations with stereotypic behaviour. The risk of horses performing abnormal behaviour increased: 1) as the amount of forage fell below 6.8 kg/day, 2) when bedding types other than straw were used, 3) when the total number of horses on the yard was fewer than 75, 4) in association with box designs that minimised contact between neighbouring horses, 5) when hay, rather than other types of forage, was used.
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Hothersall, B., & Nicol, C. (2009). Role of Diet and Feeding in Normal and Stereotypic Behaviors in Horses. Clinical Nutrition, 25(1), 167–181.
Abstract: This article reviews the effects of diet on equine feeding behavior and feeding patterns, before considering the evidence that diet affects reactivity in horses. A growing body of work suggests that fat- and fiber-based diets may result in calmer patterns of behavior, and possible mechanisms that may underpin these effects are discussed. In contrast, there is little evidence that herbal- or tryptophan-containing supplements influence equine behavior in any measurable way. The role of diet in the development of abnormal oral behaviors, particularly the oral stereotypy crib-biting, is also reviewed, and suggestions for future work are presented.
Keywords: Equine behavior; Diet; Crib-biting; Stereotypy; Weaning; Tryptophan; Insulin
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Nicol, C. J., Adachi, M., Akiyama, T. E., & Gonzalez, F. J. (2005). PPARgamma in endothelial cells influences high fat diet-induced hypertension. Am J Hypertens, 18(4 Pt 1), 549–556.
Abstract: BACKGROUND: Peroxisome proliferator-activated receptor gamma (PPARgamma) ligands improve human hypertension. However, the mechanism and site of this effect remains unknown, confounded by PPARgamma expression in many cell types, including endothelial cells (ECs). METHODS: To evaluate the vascular role of PPARgamma we used a conditional null mouse model. Specific disruption of PPARgamma in ECs was created by crossing Tie2-Cre+ transgenic (T2T+) and PPARgamma-floxed (fl/fl) mice to generate PPARgamma (fl/fl)T2T+ (PPARgamma E-null) mice. Conscious 8- to 12-week-old congenic PPARgamma (fl/fl)Cre- (wild type) and PPARgamma E-null mice were examined for changes in systolic blood pressure (BP) and heart rate (HR), untreated, after 2 months of salt-loading (drinking water), and after treatment for 3 months with high fat (HF) diet alone or supplemented during the last 2 weeks with rosiglitazone (3 mg/kg/d). RESULTS: Untreated PPARgamma E-nulls were phenotypically indistinguishable from wild-type littermates. However, compared to similarly treated wild types, HF-treated PPARgamma E-nulls had significantly elevated systolic BP not seen after normal diet or salt-loading. Despite sex-dependent baseline differences, salt-loaded and HF-treated PPARgamma E-nulls of either sex had significantly elevated HR versus wild types. Interestingly, rosiglitazone improved serum insulin levels, but not HF diet-induced hypertension, in PPARgamma E-null mice. CONCLUSIONS: These results suggest that PPARgamma in ECs not only is an important regulator of hypertension and HR under stressed conditions mimicking those arising in type 2 diabetics, but also mediates the antihypertensive effects of rosiglitazone. These data add evidence supporting a beneficial role for PPARgamma-specific ligands in the treatment of hypertension, and suggest therapeutic strategies targeting ECs may prove useful.
Keywords: Administration, Oral; Animals; Antihypertensive Agents/pharmacology; Blood Pressure/drug effects; Diabetes Mellitus, Type 2/physiopathology; Dietary Fats/*administration & dosage/pharmacology; Dose-Response Relationship, Drug; Endothelial Cells/*metabolism; Female; Heart Rate/drug effects; Hypertension/*etiology; Ligands; Male; Mice; Mice, Knockout; PPAR gamma/*metabolism; Sodium Chloride/administration & dosage/pharmacology; Thiazolidinediones/pharmacology
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Harman, F. S., Nicol, C. J., Marin, H. E., Ward, J. M., Gonzalez, F. J., & Peters, J. M. (2004). Peroxisome proliferator-activated receptor-delta attenuates colon carcinogenesis. Nat Med, 10(5), 481–483.
Abstract: Peroxisome proliferator-activated receptor-delta (PPAR-delta; also known as PPAR-beta) is expressed at high levels in colon tumors, but its contribution to colon cancer is unclear. We examined the role of PPAR-delta in colon carcinogenesis using PPAR-delta-deficient (Ppard(-/-)) mice. In both the Min mutant and chemically induced mouse models, colon polyp formation was significantly greater in mice nullizygous for PPAR-delta. In contrast to previous reports suggesting that activation of PPAR-delta potentiates colon polyp formation, here we show that PPAR-delta attenuates colon carcinogenesis.
Keywords: Animals; Azoxymethane/toxicity; Colonic Neoplasms/etiology/genetics/*prevention & control; Colonic Polyps/etiology/genetics/pathology/prevention & control; Disease Models, Animal; Mice; Mice, Knockout; Mice, Mutant Strains; Phenotype; Receptors, Cytoplasmic and Nuclear/deficiency/genetics/*physiology; Transcription Factors/deficiency/genetics/*physiology
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Dixon, G., Green, L. E., & Nicol, C. J. (2006). Effect of diet change on the behavior of chicks of an egg-laying strain. J Appl Anim Welf Sci, 9(1), 41–58.
Abstract: Injurious pecking has serious welfare consequences in flocks of hens kept for egg laying, especially when loose-housed. Frequent diet change is a significant risk for injurious pecking; how the mechanics of diet change influence pecking behavior is unknown. This study investigated the effect of diet change on the behavior of chicks from a laying strain. The study included a 3-week familiarity phase: 18 chick pairs received unflavored feed (Experiment 1); 18 pairs received orange oil-flavored (Experiment 2). All chicks participated in a dietary preference test (P); a diet change (DC); or a control group (C), 6 scenarios. All P chicks preferred unflavored feed. In Experiment 1, DC involved change from unflavored to orange-flavored; Experiment 2, orange- flavored to unflavored. Compared with controls, Experiment 2 DC chicks exhibited few behavioral differences; Experiment 1 DC chicks exhibited increased behavioral event rates on Days 1 and 7. They pecked significantly longer at their environment; by Day 7, they showed significantly more beak activity. There was little evidence of dietary neophobia. Change from more preferred to less preferred feed led to increased activity and redirected pecking behavior.
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Guo, G. L., Moffit, J. S., Nicol, C. J., Ward, J. M., Aleksunes, L. A., Slitt, A. L., et al. (2004). Enhanced acetaminophen toxicity by activation of the pregnane X receptor. Toxicol Sci, 82(2), 374–380.
Abstract: The pregnane X receptor (PXR) is a ligand-activated transcription factor and member of the nuclear receptor superfamily. Activation of PXR represents an important mechanism for the induction of cytochrome P450 3A (CYP3A) enzymes that can convert acetaminophen (APAP) to its toxic intermediate metabolite, N-acetyl-p-benzoquinone imine (NAPQI). Therefore, it was hypothesized that activation of PXR plays a major role in APAP-induced hepatotoxicity. Pretreatment with the PXR activator, pregnenolone 16alpha-carbonitrile (PCN), markedly enhanced APAP-induced hepatic injury, as revealed by increased serum ALT levels and hepatic centrilobular necrosis, in wild-type but not in PXR-null mice. Further analysis showed that following PCN treatment, PXR-null mice had lower CYP3A11 expression, decreased NAPQI formation, and increased maintenance of hepatic glutathione content compared to wild-type mice. Thus, these results suggest that PXR plays a critical role in APAP-induced hepatic toxicity, probably by inducing CYP3A11 expression and hence increasing bioactivation.
Keywords: Acetaminophen/pharmacokinetics/*toxicity; Analgesics, Non-Narcotic/pharmacokinetics/*toxicity; Animals; Aryl Hydrocarbon Hydroxylases/biosynthesis; Biotransformation; Blotting, Northern; Chromatography, High Pressure Liquid; Cytochrome P-450 CYP3A; Membrane Proteins; Mice; Mice, Knockout; Oxidoreductases, N-Demethylating/biosynthesis; Pregnenolone Carbonitrile/pharmacology; Receptors, Cytoplasmic and Nuclear/*drug effects; Receptors, Steroid/*drug effects; Sulfhydryl Compounds/metabolism
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Crosby, M. B., Zhang, J., Nowling, T. M., Svenson, J. L., Nicol, C. J., Gonzalez, F. J., et al. (2006). Inflammatory modulation of PPAR gamma expression and activity. Clin Immunol, 118(2-3), 276–283.
Abstract: Nitric oxide (NO) production increases with age in the lupus-prone MRL/lpr mouse, paralleling disease activity. One mechanism for excess NO production in MRL/lpr mice may be a defect in down-regulatory mechanisms of the iNOS pathway. A potential modulator of NO is the nuclear hormone receptor peroxisome proliferation activated receptor gamma (PPARgamma). We demonstrate that renal PPARgamma protein expression was altered as disease progressed in MRL/lpr mice, which paralleled increased iNOS protein expression. Additionally, MRL/lpr-derived primary mesangial cells expressed less PPARgamma than BALB/c mesangial cells and produced more NO in response to LPS and IFNgamma. Furthermore, PPARgamma activity was reduced in mesangial cells following exposure to inflammatory mediators. This activity was restored with the addition of a NOS enzyme inhibitor. These results indicate that the activation of inflammatory pathways may lead to reduced activity and expression of PPARgamma, further exacerbating the disease state.
Keywords: Age Factors; Animals; Cell Line, Transformed; Cells, Cultured; Female; Inflammation Mediators/*physiology; Kidney/metabolism; Mesangial Cells/metabolism; Mice; Mice, Inbred BALB C; Mice, Inbred C57BL; Mice, Inbred MRL lpr; Mice, Knockout; Nitric Oxide/biosynthesis; Nitric Oxide Synthase Type II/biosynthesis/genetics; PPAR gamma/*biosynthesis/*genetics/metabolism; Up-Regulation/immunology
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Nicol, C. J. (2004). Development, direction, and damage limitation: social learning in domestic fowl. Learn Behav, 32(1), 72–81.
Abstract: This review highlights two areas of particular interest in the study of social learning in fowl. First, the role of social learning in the development of feeding and foraging behavior in young chicks and older birds is described. The role of the hen as a demonstrator and possible teacher is considered, and the subsequent social influence of brood mates and other companions on food avoidance and food preference learning is discussed. Second, the way in which work on domestic fowl has contributed to an understanding of the importance of directed social learning is examined. The well-characterized hierarchical social organization of small chicken flocks has been used to design studies which demonstrate that the probability of social transmission is strongly influenced by social relationships between birds. The practical implications of understanding the role of social learning in the spread of injurious behaviors in this economically important species are briefly considered.
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